In a normal lung, the PAO2 rapidly increases, and it provides the gradient for transfer of O2 into capillary blood. This is associated with a marked increase in PaO2 (see 23.2 ). Similarly, over the 15-minute period of breathing enriched with O2, even areas with very low V̇ /Q̇ ratios develop high alveolar O2 pressure as the N2 is replaced by O2. In the presence of normal perfusion to these areas, there is a gradient for gas exchange, and the end-capillary blood is highly enriched with O2. In contrast, in the presence of a right-to-left shunt, oxygenation is not corrected because mixed venous blood continues to flow through the shunt and mix with blood that has perfused normal units. The poorly oxygenated blood from the shunt lowers the arterial O2 content and maintains the AaDO2. An elevated AaDO2 during a properly conducted study with 100% O2 signifies the presence of a shunt (anatomical or physiological); the magnitude of the AaDO2 can be used to quantify the proportion of the cardiac output that is being shunted.
The regional differences in ventilation and perfusion and the relationship between ventilation and perfusion were discussed earlier in this chapter. The effects of various physiological abnormalities (e.g., shunt, V̇ /Q̇ mismatch, and hypoventilation) on arterial O2 and CO2 levels were also described. In addition, however, it should be noted that because the V̇ /Q̇ ratio varies in different regions of the lung, the end-capillary blood coming from these regions has different O2 and CO2 levels. These differences are shown in
Fig. 23.7 , and they demonstrate the complexity of the lung. First, recall that the volume of the lung at the apex is less than the volume at the base. As previously described, ventilation and perfusion are less at the apex than at the base, but the differences in perfusion are greater than the differences in ventilation. Thus the V̇ /Q̇ ratio is high at the apex and low at the base. This difference in ventilation/perfusion ratios is associated with a difference in alveolar O2 and CO2 content between the apex and the base. The PAO2 is higher and the PACO2 is lower in the apex than in the base. This results in differences in end-capillary contents for these gases. End-capillary PO2 is lower, and, as a consequence, the O2 content is lower in end-capillary blood at the lung base than at the apex. In addition, there is significant variation in blood pH in the end capillaries in these regions because of the variation in CO2 content. During exercise, blood flow to the apex increases and becomes more uniform in the lung; as a result, the difference between the content of gases in the apex and in the base of the lung diminishes with exercise.
1.
The volume of air in the conducting airways is called the anatomical dead space. Dead space ventilation varies inversely with tidal volume. The total volume of gas in each breath that does not participate in gas exchange is called the physiological dead space. It includes the anatomical dead space and the dead space secondary to ventilated but unperfused alveoli.
2.
The sum of the partial pressures of a gas is equal to the total pressure. The partial pressure of a gas (Pgas) is equal to the fraction of the gas in the gas mixture (Fgas) multiplied by the total pressure (Ptotal). The conducting airways do not participate in gas exchange. Therefore, the partial pressures of O2, N2, and water vapor in humidified air remain unchanged in the airways until the gas reaches the alveolus.
3.
The partial pressure of O2 in the alveolus is given by the alveolar air equation (
Eq. 23.13 ). This equation is used to calculate the AaDO2, a useful measurement of abnormal arterial O2.
4.
The relationship between CO2 production and alveolar ventilation is defined by the alveolar carbon